FcγRIIb Inhibits Allergic Lung Inflammation in a Murine Model of Allergic Asthma 英文参考文献.docVIP
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FcγRIIb Inhibits Allergic Lung Inflammation in a Murine Model of Allergic Asthma 英文参考文献
FccRIIbInhibitsAllergicLungInflammationinaMurine
ModelofAllergicAsthma
NileshDharajiya1,SwapnilV.Vaidya2,HirokiMurai2,VictorCardenas2,AlexanderKurosky3 ,Istvan
Boldogh4,SanjivA.Sur2*
1NationalHeart,Lung,andBloodInstitute(NHLBI)ProteomicsCenter,DepartmentofBiochemistryandMolecularBiology,UniversityofTexasMedicalBranch,Galveston,
Texas, United States ofAmerica, 2Departmentof Internal Medicine, University of TexasMedicalBranch, Galveston, Texas, United States of America, 3Department of
BiochemistryandMolecularBiology,UniversityofTexasMedicalBranch,Galveston,Texas,UnitedStatesofAmerica,4DepartmentofMicrobiology,UniversityofTexas
MedicalBranch,Galveston,Texas,UnitedStatesofAmerica
Abstract
Allergic asthma is characterized by airway eosinophilia, increased mucinproduction andallergen-specific IgE. Fcgamma
receptor IIb (FccRIIb), an inhibitory IgG receptor, has recently emerged as a negative regulator of allergic diseases like
anaphylaxisandallergicrhinitis.However,nostudiestodatehaveevaluateditsroleinallergicasthma.Ourmainobjective
wastostudytheroleofFccRIIbinallergic lunginflammation.Weused amurine modelofallergicairwayinflammation.
InflammationwasquantifiedbyBALinflammatorycellsandairwaymucinproduction.FccRIIbexpressionwasmeasuredby
qPCR andflow cytometryandthecytokineswerequantifiedby ELISA.Compared towildtypeanimals,FccRIIb deficient
mice mount a vigorous allergic lung inflammation characterized by increased bronchoalveolar lavage fluid cellularity,
eosinophilia and mucin content upon ragweed extract (RWE) challenge. RWE challenge in sensitized mice upregulated
FccRIIbinthelungs.DisruptionofIFN-cgeneabrogatedthisupregulation.Treatmentofna?¨vemicewiththeTh1-inducing
agentCpGDNAincreasedFccRIIbexpressioninthelungs.Furthermore,treatmentofsensitizedmicewithCpGDNApriorto
RWEchallengeinducedgreaterupregulationofFccRIIbthanRWEchallengealone.TheseobservationsindicatedthatRWE
challengeupregulatedFccRIIbinthelungsbyIFN-c-andTh1-dependentmechanisms.RWEchallengeupreg
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